Infants born with fetal alcohol syndrome (FAS) often present with a wide variety of immunologic anomalies affecting both the humoral and cell mediated arms of the immune system. Recent work from this lab suggests that in utero exposure to ethanol causes a delay in B cell development in neonatal mice. In addition, we noted the accumulation of a cell, that had the phenotype of low expression for heat stable antigen (HsA1o and negative for the pan B cell marker B220 (B220-), in the spleen and bone marrow of ethanol exposed neonatal mice. Preliminary characterization of this cell type by flow cytometry revealed a cell type that was 'lymphoid like' in both size and granularity. The HSA1oB22O- population of cells represented 10-12% of adult bone marrow and about 16% of neonatal bone marrow. When these cells were isolated and placed in culture with stromal cells and IL-7 some were able to differentiate into B220+ cells suggesting that within this population of cells resides a progenitor of the B cell lineage. The aberrant expression of these progenitor like cells in ethanol exposed neonatal mice may reveal a mechanism for the delay we observe in B cell development. It is the goal of this proposal to characterize the HSA1oB220- cell type, paying particular attention to the developmental capabilities both in vivo and in vitro.